New approaches to preventing restenosis
BMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7409.274 (Published 31 July 2003) Cite this as: BMJ 2003;327:274All rapid responses
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with the astronomical rise in number of angioplasties with stenting,
coronary restenosis of 10-30% is the interventional cardiologist's
Achilles' heel.the major cause of restenosis appears to be neo-intimal
proliferation.aiming at near zero percent restenosis have opened the
pandora's box of big money with 'high technology' competitive procedures
like coronary brachytheraphy and drug eluting stents.the costs of these
procedures are prohibitive and not without disconcerting fall outs like
edge effect, in situ thrombosis, aneurysm, and in one case pseudo-aneurysm
formation.
i think there is a need to also look at less expensive alternatives. one
important development in the field of contrast echocardiography is the
potential ability to deliver adherent drugs or genes by use of
microbubbles.PESDA microbubbles can deliver genes and possible other anti-
proliferative agents to injured sites within coronary artery to prevent
neo-intimal hyperplasia.
another area is the use of macrolide antibiotics. mycoplasma pneumoniae
has been implicated in atherogenesis. its use can stabilise plaques. its
recent use after PCI in those with high titres of mycoplasma antibodies
led to a reduction in rate of coronary restenosis.
a growing body beleive that statins may have a role to play in PCI. the
statins have actions beyond their lipid lowering effect. they may have a
role to play as anti-inflammatory agents useful when given thru a PCI,
improving procedural success.whether they reduce restenosis rate after PCI
has not been reported.
homocystein is also beleived to be an important factor in plaque
production. studies have shown that folates do reduce restenosis rate
after PCI.
ace inhibitors which block activation of renin-angiotensin system have
majot effect on development and progression of atherosclerosis. they are
also anti-proliferative. they may be useful in preventing restenosis,
although one study showed a paradoxical result.
Competing interests:
None declared
Competing interests: No competing interests
There is a place for medical treatment to prevent restenosis
The recent review of new approaches to preventing stent restenosis by
Bhargava et al (1) did not , in our opinion, give an adequate
representation of the role of medical therapy in the prevention of stent
restenosis. The authors state that the role of drugs "is likely to be
small" and that "their contribution is largely disappointing". We believe
that this is not consistent with the results of the data in the
literature.
Elevations of homocysteine have been shown to be related to an increased
risk of adverse outcomes and target lesion revascularization after
percutaneous coronary intervention (2) More impressively, reduction of
serum homocysteine levels by the addition of a combination of folic acid,
vitamin B12 and vitamin B6 in a trial of 553 patients reduced the
composite end point at one year (primarily due to a reduction in target
vessel revascularization) from 16.6% to 9.9% (3). This is an impressive
reduction. However, only 54% of these patients received a stent and only
56% received either clopidrogel or ticlopidine. It remains to be seen what
the role is of homocysteine reduction in patients with drug-eluting
stents.
The routine use of clopidrogel or ticlopidine prior to and following
angioplasty and placement of a stent is now well accepted. A recent meta-
analysis (4) of clopidrogel and ticlopidine use after stent deployment
concluded that clopidrogel and aspirin should be the standard antiplatelet
regimen following stent deployment.
The use of glycoprotein IIb/IIIa blockade following stent deployment has
also been shown to be effective. In the EPISTENT trial (5), the risk of
the primary endpoint of death, MI or urgent revascularization was achieved
in 10.8% in the stented plus placebo group versus 5.1% in the stent plus
abiciximab group.
In addition, it is important to remember that coronary stenting treats the
affected vessel but offers no therapy for the other coronary vessels which
may be affected at a later date.
In summary, there is ample evidence in the literature to support medical
therapy after coronary stent deployment and we feel this should have
received more attention in the review by Bhargava et al.
References.
1. Bhargava B, Kathrikeyan G, Abizaid AA, Mehran A. New approaches to
preventing restenosis. BMJ 2003; 327: 274-279.
2. Schnyder G, Flammer Y, Roffi M, Pin R, Hess OM. Plasma homocysteine
levels and late outcome after coronary angioplasty. J Am Coll Cardiol
2002; 40:1769-76.
3. Schnyder G, Roffi M, Flammer Y, Pin R, Hess OM. Effect of homocysteine-
lowering therapy with folic acid, vitamin B12 and vitamin B6 on clinical
outcome after percutaneous coronary intervention : the Swiss heart study:
a randomized controlled trial. JAMA 2002; 288:973-9.
Competing interests:
None declared
Competing interests: 5. Lincoff AM, Califf RM, Moliterno DJ, Ellis SG, Ducas J et al. Complementary clinical benefits of coronary-artery stenting and clinical blockade of platelet glycoprotein IIa/ receptors. Evaluation of platelet IIb/IIIa inhibition in stent investigators. N Engl J Med 1999; 341: 319-27.